What Is Ventricular Tachycardia?

Ventricular tachycardia (VT) refers to the tachyarrhythmias of the bundle branches, myocardial conductive fibers, and ventricular muscles that occur below the bifurcation of the His bundle, and Wellens defines it as: frequency more than 100 times / min, 3 consecutive Or more than 3 spontaneous ventricular electropolar depolarization activities, including single-form non-persistent and continuous ventricular tachycardia and polymorphic ventricular tachycardia, if induced by electrical cardiac stimulation during cardiac electrophysiology Ventricular tachycardia must be sustained ventricular tachycardia with a frequency of 6 or more (frequency> 100 beats / min). Ventricular tachycardia can originate from the left ventricle and the right ventricle. Frequent episodes of frequent tachycardia often exceed 100 beats / min, and can deteriorate the hemodynamic state, which may degenerate into ventricular flutter, ventricular fibrillation, and cause the heart. Sudden death requires active treatment.

Basic Information

English name

ventricular tachycardia, VT

Visiting department

cardiology

Multiple groups

Patients with organic heart disease

Common locations

heart

Common causes

Organic heart disease, electrolyte disorders and acid-base balance disorders, drug and poison effects, etc.

Common symptoms

Palpitation, chest tightness, chest pain, dark, syncope, increased heart rate, restlessness, fear, etc.

Causes of ventricular tachycardia

According to the duration, ventricular tachycardia is divided into: continuous ventricular tachycardia (onset time greater than 30 seconds) and non-sustained ventricular tachycardia (onset time less than 30 seconds). In addition, it can be classified according to the presence or absence of organic heart disease, ECG morphology of ventricular tachycardia, the origin of VT, and post-healing.

1. Ventricular tachycardia caused by organic heart disease

(1) Coronary heart disease Ventricular tachycardia can occur in various types of coronary heart disease such as acute myocardial infarction, old myocardial infarction, angina pectoris or painless myocardial ischemia. Acute myocardial ischemia can cause reentry activity induced by delayed myocardial agitation in the ischemic area. Old myocardial infarction is often the reentry of myocardial formation in the scar area at the margin of the infarction. The pathological basis of ventricular tachycardia in patients with myocardial infarction is mainly the significant abnormal wall motion, the formation of left ventricular wall tumors, and the significant left ventricular dysfunction.

(2) Ventricular tachycardia can occur in primary cardiomyopathy, dilated cardiomyopathy, hypertrophic cardiomyopathy, and restricted cardiomyopathy. Myocardial cell necrosis, fibrosis, and lesions in patients with primary cardiomyopathy. The myocardium loses its normal structure and morphology, causing conduction disturbances to form reentry, causing ventricular tachycardia.

(3) Mitral valve prolapse Ventricular tachycardia originates from the breast muscle and annulus, often caused by reentry, and is mostly monomorphic VT. Polymorphic ventricular tachycardia is mostly caused by increased autonomy or triggered activity, and is considered to be a mechanism that causes sudden cardiac death.

(4) Myocarditis is often a common cause of ventricular tachycardia.

In addition, hypertensive heart disease, heart valve disease, and congenital heart disease can also cause different degrees of ventricular tachycardia.

2. Ventricular tachycardia without organic heart disease

(1) Electrolyte disorders and acid-base balance disorders such as hypokalemia, hyperkalemia, hypomagnesemia, and acidosis often cause ventricular tachycardia. Ventricular tachycardia is more likely to occur if combined with organic heart disease .

(2) Drugs and poisons Digitalis drugs, antiarrhythmic drugs quinidine, sympathomimetic drugs, penicillin allergy, etc.

(3) Idiopathic ventricular tachycardia refers to ventricular tachycardia in patients without significant organic heart disease. The majority of young adults may have heart disease, and the idiopathic nature is relatively speaking.

Clinical manifestations of ventricular tachycardia

Symptoms

The clinical manifestations of ventricular tachycardia are not consistent. Patients may experience palpitation, chest tightness, chest pain, darkening, and syncope. The clinical features are sudden onset, and suddenly disappear after treatment or self-limitation. When the attack occurs, the patient suddenly feels palpitations, rapid heart rate, nervousness, fear, and discomfort in the precardiac area Swelling and throbbing head or neck. People with non-sustained ventricular tachycardia are usually asymptomatic and are only found on a physical examination or 24-hour electrocardiogram.

2. Signs

The auscultation heart rate is slightly irregular. The first and second heart sounds are split. The systolic blood pressure can change with the heartbeat. If complete atrioventricular separation occurs, the first heart sound intensity often changes, and the jugular vein intermittently displays a huge a wave. The atrial was continuously captured by back pass, and the atria and ventricles contracted almost simultaneously. The jugular vein showed a regular and huge a wave.

Ventricular tachycardia

1. Patients without organic heart disease should check blood potassium, blood magnesium, pH and so on.

2. The electrocardiogram showed the characteristics of typical ventricular tachycardia.

Differential diagnosis of ventricular tachycardia

1. Differentiated from supraventricular tachycardia (referred to as supraventricular tachycardia) with QRS complex widening (the existing bundle branch block)

(1) When the supraventricular velocity is associated with left bundle branch or right bundle branch block, the wide QRS waveform should present a typical bundle branch block pattern. If the supraventricular beam is accompanied by a left beam block, the electrical axis should be left-biased. Leads V ₁ and V ₂ should be of the rS type. The r-wave interval should be <30 ms. The Q ₅ and V ₆ leads should not have q waves. Previous electrocardiograms or electrocardiograms that restore sinus rhythm have important significance for the diagnosis of supraventricular tachycardia with the original bundle branch block.

(2) The differentiation of supraventricular tachycardia with continuous differential conduction and ventricular tachycardia is difficult. The occurrence of differential conduction can be a functional change of the intraventricular bundle branch or a pathological change. The right bundle branch block type can be found in healthy people and patients with organic heart disease, while the left bundle branch block type is more common in patients with organic heart disease and rarely seen in healthy people.

2. Identification with reverse atrioventricular tachycardia

Retrograde atrioventricular reentrant tachycardia, that is, atrioventricular reentrant tachycardia, which is passed through the atrium. The atrial excitement passes down the ventricle to the ventricle. The ventricular excitement then passes from the atrioventricular node to the atrium. The ventricle is excited by the bypass. The QRS wave is wide and deformed. Its frequency is above 220 beats / min, and the frequency of ventricular tachycardia is mostly 100-220 beats / min, and it is rare to exceed 220 beats / min.

3. Identification of AF with preexcitation syndrome (preexcitation):

(1) When atrial fibrillation occurs in preexcitation syndrome, a wide deformed QRS wave tachycardia appears, but there are also narrow QRS wave groups or ventricular fusion waves, which change the shape of the QRS wave before and after the ECG.

(2) When atrial fibrillation is combined with pre-excitation, the P-waves of atrial fibrillation disappear, and the RR intervals are absolutely different. After the sinus rhythm is restored, the pre-excitation wave can be seen on the ECG.

(3) Atrial fibrillation is associated with WPW syndrome. Atrial fibrillation is often caused by atrioventricular reentry. After ablation bypass treatment, most patients no longer have atrial fibrillation.

Ventricular tachycardia treatment

Ventricular tachycardia occurs mostly in people with heart disease, which can cause serious consequences and increase mortality. Active treatment is needed to stop the onset of ventricular tachycardia immediately. Its treatment principles: Once ventricular tachycardia occurs, the attack should be terminated immediately. Eliminate incentives, pay attention to the use of hypokalemia, digitalis drugs. Actively treat the primary disease, such as the correction of heart failure and the treatment of ventricular wall tumors after myocardial infarction. Prevent recurrence of ventricular tachycardia. After termination of ventricular tachycardia, medication or non-drug measures should be used to prevent recurrence of ventricular tachycardia. Prevention and treatment of sudden cardiac death.

1. Ventricular tachycardia drug treatment

The preferred method to stop persistent ventricular tachycardia is to immediately inject intravenous antiarrhythmic drugs. For monomorphic ventricular tachycardia or polymorphic ventricular tachycardia with normal QT interval, drug treatment is generally used. Intravenous injection. lidocaine; amiodarone; propafenone, choose one of them, and continue to inject the above drugs if it is effective. The treatment of polymorphic ventricular tachycardia is similar to that of monomorphic, but it should be carefully searched for possible reversible causes, such as drug side effects and electrolyte disturbances, especially the tip-torsional ventricular tachycardia, which mostly occurs between QT When the period is extended. In addition to the cause of the treatment, isoproterenol, atropine intravenous injection, or rapid artificial heart pacing can be used. Class III antiarrhythmic drugs, such as amiodarone, are avoided. Intravenous administration of high-dose magnesium sulfate is effective for patients with refractory ventricular tachycardia and ventricular fibrillation, apical torsional ventricular tachycardia, and digitalis poisoning. The use of magnesium in patients without digitalis poisoning may produce hypokalemia, so potassium supplementation is also required.

2. Non-drug treatment of ventricular tachycardia

(1) The principle of direct current cardioversion is that after all cells in the reentry loop are depolarized, the ECG identity is generated, and the reentry loop no longer exists. A large number of practices have proved that DC cardioversion is a very safe and effective treatment for termination of ventricular tachycardia. In many cases, it should be used as the first choice, convenient and efficient.

(2) Radiofrequency ablation is currently mainly used for the treatment of idiopathic ventricular tachycardia, bundle branch reentry ventricular tachycardia, etc., with fewer surgical complications, and can cure VT. For concurrent cardiac structural lesions, such as dilated cardiomyopathy, the origin of tachycardia is often a more diffuse lesion, and radiofrequency ablation is more difficult. For ventricular tachycardia after myocardial infarction, radiofrequency ablation has certain effects.

(3) Implantation of an embedded cardioversion defibrillator can immediately and effectively terminate the onset of ventricular tachycardia, and is by far the most effective means of reducing sudden cardiac death.

(4) Surgery For some refractory ventricular tachycardia, surgical treatment is available, such as resection of the wall tumor, partial removal of the enlarged left ventricle, and so on.

Ventricular tachycardia prevention

Ventricular tachycardia is a very serious arrhythmia and must be prevented. Efforts should be made to find and treat various reversible lesions that induce and maintain ventricular tachycardia, such as ischemia, hypotension, and hypokalemia. Treatment of heart failure can help reduce the number of ventricular tachycardia episodes. When sinus bradycardia or atrioventricular block occurs, the ventricular rate is slow and ventricular tachycardia is prone to occur. Atropine can be given or artificial heart pacing can be applied.